Blossom end rot is a troublesome disease, familiar to most gardeners who have grown tomatoes. The disease is often prevalent in commercial as well as home garden tomatoes, and severe losses may occur if preventive control measures are not undertaken.
Symptoms may occur at any stage in the development of the fruit, but, most commonly, are first seen when the fruit is one-third to one-half full size. As the name of the disease implies, symptoms appear only at the blossom end of the fruit. Initially a small, water-soaked spot appears, which enlarges and darkens rapidly as the fruits develop. The spot may enlarge until it covers as much as one third to one-half of the entire fruit surface, or the spot may remain small and superficial. Large lesions soon dry out and become flattened, black, and leathery in appearance and texture.
This disease does not spread from plant to plant in the field, nor from fruit to fruit in transit. Since it is of a physiological nature, fungicides and insecticides are useless as control measures. The occurrence of the disease is dependent upon a number of environmental conditions, especially those that affect the supply of water and calcium in the developing fruits. Factors that influence the uptake of water and calcium by the plant have an effect on the severity of blossom end rot. The disease is especially prevalent when rapidly growing, succulent plants are exposed suddenly to a period of drought. When the roots fail to obtain sufficient water and calcium to be transported up to the rapidly developing fruits, the latter become rotted on their basal ends. Another common factor is cultivation too close to the plant; this practice destroys valuable roots, which take up water and minerals. Tomatoes planted in cold, heavy soils often have poorly developed root systems. Since they are unable to supply adequate amounts of water and nutrients to plants during times of stress, blossom end rot may result. Soils that contain excessive amounts of soluble salts may predispose tomatoes to the disease, for the availability of calcium to the plants decreases rapidly as total salts in the soil increase.
Control
Control of blossom end rot is dependent upon maintaining adequate supplies of moisture and calcium to the developing fruits. Tomatoes should not be excessively hardened nor too succulent when set in the field. They should be planted in well drained, adequately aerated soils. Tomatoes planted early in cold soil are likely to develop blossom end rot on the first fruits, with the severity of the disease often subsiding on fruits set later. Thus, planting tomatoes in warmer soils helps to alleviate the problem. Irrigation must be sufficient to maintain a steady even growth rate of the plants. Mulching of the soil is often helpful in maintaining adequate supplies of soil water in times of moisture stress. When cultivation is necessary, it should not be too near the plants nor too deep, so that valuable feeder roots remain uninjured and viable. In home gardens, shading the plants is often helpful when hot, dry winds are blowing, and soil moisture is low. Use of fertilizer low in nitrogen, but high in super phosphate, such as 4-12-4 or 5-20-5, will do much to alleviate the problem of blossom end rot. In emergency situations, foliage can be sprayed with calcium chloride solutions. However, extreme caution must be exercised since calcium chloride can be phytotoxic if applied too frequently or in excessive amounts. Foliar treatment is not a substitute for proper treatment of the soil to maintain adequate supplies of water and calcium.
Early Blight
Early blight (EB) is a disease of potato caused by the fungus Alternaria solani. It is found wherever potatoes are grown. The disease primarily affects leaves and stems, but under favorable weather conditions, and if left uncontrolled, can result in considerable defoliation and enhance the chance for tuber infection. Premature defoliation may lead to considerable reduction in yield. The disease can also be severe on tomatoes, and can occur on other solanaceous crops and weeds.
DISEASE CYCLE
The fungus overwinters either on potato tubers or in dead, infected plant debris either in the soil or on the soil surface. Therefore, primary infection is difficult to predict since EB is less dependent upon specific weather conditions than late blight. Environmental factors and plant vigor also help to determine when the first EB lesions are found. Infection can occur from early to mid July when frequent rains or dews occur and daytime temperatures remain near 75-80 F. The fungus can penetrate the leaf surface directly through the epidermis and spots begin appearing in 2-3 days. Lesions are most numerous and pronounced on lower, older, and less vigorous leaves and on early maturing varieties The lesions are dark brown and appear leathery with faint, concentric rings giving a “target-spot” effect. At first the spots are small (1 /8″ in diameter) and oval or angular in shape, but later the spots can enlarge to about 1/2″. In many cases they are bounded by the larger leaf veins More spores are produced on the EB spots and lesions, greatly increasing the secondary spread of wind-borne conidia between plants and between fields. At harvest time, spores from blighted vines may be deposited onto tubers. These spores germinate during wet and warm weather and invade the tissue, primarily through cuts, bruises, or wounded surfaces.
Tuber infections appear as generally small, irregular, brownish—black spots which are usually slightly sunken (approx. 1/16″) Externally the spots resemble those caused by late blight, but internally they are shallower and darker in color. The rotted tuber tissue is firm, hard, and somewhat corky. EB tuber rot develops slowly and may not be severe until quite late into the storage period. This decay may allow the entry of secondary organisms such as Fusarium fungi and soft rot bacteria.
CONTROL
The following measures will help prevent the occurrence of serious EB outbreaks, (1) Plant only diseasefree, certified seed. (2) Follow a complete and regular foliar fungicide spray program. (3) Practice good killing techniques to lessen tuber infections. (4) Allow tubers to mature before digging, dig when vines are dry, not wet, and avoid excessive wounding of potatoes during harvesting and handling. (5) Plow under all plant debris and volunteer potatoes after harvest. (6) Avoid replanting potatoes (and tomatoes or eggplants) in the affected area for at least 2 years if severe outbreaks have been experienced. (7) Although no cultivar is immune to EB, several cultivars are moderately resistant and should be planted if blight is a continuing problem.
Late Blight
Late blight of potatoes and tomatoes, the disease that was responsible for the Irish potato famine in the mid-nineteenth century, is caused by the fungus-like oomycete pathogen Phytophthora infestans. It can infect and destroy the leaves, stems, fruits, and tubers of potato and tomato plants. Before the disease appeared in Ireland it caused a devastating epidemic in the early 1840s in the northeastern United States.
P. infestans was probably introduced to the United States from central Mexico, which is its center of origin. After appearing in North America and Europe during the 1840s, the disease spread throughout most of the rest of the world during subsequent decades and had a worldwide distribution by the beginning of the twentieth century.
Severe late blight epidemics occur when P. infestans grows and reproduces rapidly on the host crop. Reproduction occurs via sporangia that are produced from infected plant tissues and is most rapid during conditions of high moisture and moderate temperatures (60°-80°F). Sporangia disperse to healthy tissues via rain splash or on wind currents. Reproduction is asexual; each sporangium is an exact copy of the one that initiated the parent lesion, and each can initiate a new lesion.
During the early 1990s several exotic strains of P. infestans were introduced from Mexico. These strains have increased the severity of late blight on potato and tomato because they are more aggressive than earlier ones in the United States and Canada. They initiate infections more quickly and reproduce more profusely, causing epidemics to occur rapidly. To combat these strains it is necessary to use more resistant potato and tomato cultivars or to use fungicides more intensively. Unfortunately, resistance of potato foliage and stems is not necessarily related to tuber resistance. Potato cultivars with desirable market qualities and whose foliage and tubers show high levels of resistance are being developed. Traditional methods include using breeding lines or cultivars as sources of resistance; new methods include using wild species as sources of resistance and employing molecular techniques in which genes responsible for resistance are transferred into potato cultivars via genetic engineering techniques.
Though some commercial tomato cultivars are more susceptible than others, few are resistant. Under conditions that are favorable to late blight, epidemics in tomatoes seem to be more rapid than in potatoes. Some sources of resistance have been identified in wild relatives of tomato, and efforts are being made to bring higher levels of resistance into cultivars that are desirable for the market.
DISEASE CYCLE
Usually it lives in infected potato tubers which can survive in storage or the soil (to become volunteers) after harvest or anywhere potatoes might be discarded. Tubers that have been discarded at any stage of crop production or handling (harvest, storage, shipping, spring cleanup, or planting) are known as “culls.” Culls may survive if they are not destroyed (frozen, crushed, composted, or buried at least 2 feet beneath the soil surface). Infected tubers that are planted or cull tubers that survive the winter may be sources of the pathogen that initiate epidemics the following season.
P. infestans is usually dispersed aerially one to several miles from the overwintering site to living potato or tomato foliage via sporangia and left which can survive exposure to dry, sunny conditions for up to an hour and even longer under cloudy conditions. Sporangia can germinate within a few hours after landing on potato or tomato foliage if free moisture (e.g., dew, rainfall, sprinkler irrigation, fog) is present. Germination takes place either indirectly via zoospores or directly via a germ tube that penetrates into foliage, stems, or fruit to initiate infections. Infections are visible as small lesions after three to four days. Necrotic areas on some lesions are only 1 to 2 mm in diameter Lesions enlarge as the pathogen grows through the tissues, and the pathogen can sporulate from older lesions when the environment is favorable (leaf wetness for more than 10 to 12 hours at moderate temperatures [60°-70°F). Sporulation may occur on lesions that are only four to six days old. Under dry conditions no sporulation occurs and the lesion has a brown dead center, surrounded by host tissue that has collapsed and appears either water soaked, gray-green, or yellowed . Both tomato and potato fruits are susceptible Their stems may be infected and stem lesions are capable of producing sporangia for a longer time than can lesions on leaves.
Disease development (growth and reproduction of the pathogen) is favored by moderate temperatures (60°-80°F) and wet conditions. It can develop in very warm daytime temperatures (ca. 95°F) if conditions are extremely wet and night temperatures are moderate (60°-75°F). Epidemics can be rapid and devastating because of the high reproductive potential of this pathogen. Individual lesions can produce 100,000 to 300,000 sporangia per day. Each sporangium is capable of initiating a new infection that will become visible within three to four days and produce sporangia within another day or two under optimal conditions. Thus rapid reproduction of the pathogen and destruction of leaflets can defoliate potatoes or tomatoes and completely destroy healthy fields in a short time Such epidemics result from many sequential cycles of infections: every lesion produces many sporangia, each of which can be dispersed to a new leaflet to initiate a new infection, which in turn can produce many sporangia, and so on.
Tubers may be infected by P. infestans whenever sporangia and tubers come into contact, from early in the tuberization process until harvest. Infections most commonly occur when sporangia are washed from lesions on stems and foliage to the soil and then through the soil to tubers. Infections can occur on developing or mature tubers, but contact between tubers and sporangia is more likely when the tubers are enlarging; tuber enlargement creates cracks in the soil and gives sporangia ready access. Tubers become infected most often when soils are cool and wet (near field capacity); soil temperatures higher than 65°F seem to suppress infections. Because sporangia can survive days or weeks in soil, tubers can become infected for a period of time after infections in the foliage are no longer producing sporangia.
Tubers infected by late blight are especially susceptible to soft rot. If some tubers in a crop are infected, store the crop in cool, dry conditions. If infected potatoes are stored at high relative humidity and moderate temperatures, soft rot can be severe, destroying infected tubers first but subsequently destroying previously healthy ones
Infections can probably also occur during harvest and subsequent handling. Although late blight inoculations during storage were previously considered highly unlikely, such occurrences have been documented recently.
Tomato leaflets can be destroyed at least as rapidly as potato leaflets, leading to complete defoliation in a short time.
Control
Use of integrated management practices is necessary for successful suppression of potato or tomato late blight. Therefore, sanitation elimination or exclusion of infected plants is important in the overall management strategy. Ideally, no infected potatoes should be present in the vicinity of the crop. Volunteer plants that might be infected should be destroyed. Cull potatoes should be frozen, crushed, fed to livestock, or buried under at least 2 feet of soil. Only tubers that are free of P. infestans should be planted. After planting, additional precautions will reduce the chances of successful inoculations and can suppress development and reproduction of the pathogen. Using resistant cultivars will reduce the chances of infection and slow the pathogen growth rate if some infections develop. Earthing up/Hilling of potatoes increases the amount of soil between tubers and the soil surface and thus helps protect tubers from sporangia that land on the soil surface.
Regular inspections of growing crops are important to the overall management of late blight. Because topography and crop growth can influence the microclimate encountered by the pathogen, late blight may be detectable earlier in some areas than in others. It is likely to appear first in wet areas (low spots in the field, areas adjacent to woods and hedgerows, dense crops, or areas adjacent to other features that might shade crops), especially when the macroclimate has been less than optimal for pathogen development.
Treating established infections.
Once 5 to 10 percent of the foliage is infected it is usually not possible to halt the development or progress of the disease.Only weather that is very dry and hot, both day and night, might temporarily stop the epidemic. Stem infections are very resistant to drying, however, and will sporulate when sufficient moisture is available. Growers can attempt to salvage apparently uninfected tomato fruit but should be aware that some fruit infections will not become visible for several days. Foliage that is infected should be destroyed and not composted
Another good resource
